Letter to the editor

Abstract

I read Önen et al’s article entitled “Effects of whole blood, crystalloid, and colloid resuscitation of hemorrhagic shock on renal damage in rats: an ultrastructural study” in the November 2003 issue (pp 1642–1649). The authors have shown that resuscitation of hemorrhagic shock with dextran 40 have beneficial effects on renal histology and relate this beneficial effect to reduced red cell slugging, volume expansion, and hemodilution-induced reduction in blood viscosity. However, intravital microscopic study of the intestinal mesenteric microcirculation has shown that resuscication of hemorrhagic shock with hypertonic saline solution containing dextran (HSD; 7.5% NaCl/6% dextran 70) restores microvascular blood flow better than resuscitation with an equal volume of Ringer’s lactate.1 Laser Doppler flowmetry has been used to show beneficial effects of HSD on restoration of intestinal and renal blood flows after resuscitation of hemorrhagic shock.2 Intravital microscopy has been used to show the prevention of hemorrhagic shock- induced leukocyte-endothelium adherence in liver sinusoids after resuscitation with HSD.3 Low-molecular-weight dextran has beneficial effects similar to those of high-molecular-weight dextran on microcirculation. Radioisotopic study of blood flow to multiple organs has shown that resuscitation of hemorrhagic shock with a pure solution of dextran 40 restores blood flow to these organs better than Ringer’s lactate.4 Additionally, dextran has been shown to have free oxygen radical scavenging capacity.5 Hemorrhagic shock has been shown to induce P-selection expression through free oxygen radical formation that leads to no-reflow phenomenon.6,7 Dextran 40 has been shown to prevent hemorrhagic shock-induced P-selectin expression thus abolish no-reflow phenomenon.8